The past decade has seen a reduction in deaths due to coronary artery disease form the widespread use of HMG CoA reductase inhibitors, or statins, which are used to lower LDL cholesterol. It has been suggested that not all of the reduction in morbidity and mortality, from these agents, can be attributed to reductions in LDL cholesterol. We believe that some of this additional benefit comes from endothelial activation. The endothelium is a biologically active monolayer of cells, which lines the inside wall of arteries and veins. Endothelial cells produce nitric oxide, a short-lived substance with a number of functions including vasodilatation and inhibition of platelet aggregation and adhesion. Endothelial cells function abnormally in a number of conditions including smoking, diabetes, and high cholesterol. Endothelial function can be assessed by measuring arterial vasodilatation after a period of occlusion as well as by measuring metabolites of nitric oxide and its precursors (Nox, citrulline, ornithine, arginine, ET-1). We will measure these parameters in smokers with normal LDL levels after giving them an HMG CoA reducatse inhibitor. Our goal is to determine if these agents can activate the endothelium in subjects with impaired endothelial function without affecting LDL cholesterol levels. We will start by measuring these parameters 24 and 48 hours after starting the drug. However, as this is a pilot study, we may need to alter the times of measurement during the study.